This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The goal of this study is to determine the role of hypoxic stress on the regulation of sympathetic activity and blood flow in healthy humans. Transient hypoxia acutely increases sympathetic activity and evokes vasodilation while intermittent hypoxia tends to evoke sustained sympathoexcitation and enhanced chemoreflex sensitivity. The working hypothesis of this study is that intermittent hypoxia compared to transient hypoxia will excite the sympathetic nervous system, alter sympathetic reflex function and evoke compensatory adaptations of vascular function that oppose sympathetic vasoconstrictor tone during hypoxia. Further, exercise training will reduce this effect.